Downregulation of miRNA-26b inhibits cancer proliferation of laryngeal carcinoma through autophagy by targeting ULK2 and inactivation of the PTEN/AKT pathway.

Abstract

Laryngeal carcinoma is one of the most common tumors of the head and neck cancers, the pathogenesis of which remains yet unclear. It has been discovered through research that microRNAs (miRNAs) play an important role during the genesis of laryngeal carcinoma. In the present study we investigated the effect of miRNA-26b on the proliferation of laryngeal carcinoma and elucidated the potential underlying mechanisms in order to provide new targets for laryngeal carcinoma. Firstly, we found that miRNA-26b expression was significantly increased in patients with laryngeal carcinoma, compared with normal volunteers. The downregulation of miRNA-26b inhibited cell proliferation and induced apoptosis of Hep-2 cells. Furthermore, downregulation of the expression of miRNA‑26b promoted Bax, LC3 and p62 protein expression, decreased ULK2 mRNA and protein expression, as well as PTEN protein expression and increased phosphorylated‑AKT protein expression in Hep-2 cells as determined using quantification by real-time PCR and western blotting. The concomitant downregulation of ULK2 and miRNA-26b futher enhanced the miRNA‑26b-induced autophagy and apoptosis in addition to the miRNA-26b-inhibited cell proliferation of Hep-2 cells by targeting ULK2 and inactivating the PTEN/AKT pathway as determined by immunocytofluorescence. These findings revealed that miRNA-26b may play a key role in cell growth and death of laryngeal carcinoma through ULK2 and the PTEN/AKT pathway, and thus may be a new target for gene therapy in laryngeal carcinoma.